INTRODUCTION
Atrial fibrillation (AF) is the most common cardiac tachyarrhythmia.. Its pathophysiology is complex1 and can be described with: 1) triggers for the initiation of the arrhythmia (pulmonary and non-pulmonary foci); 2) a fibrotic substrate for the maintenance of AF; and 3) various modulators acting by multiple potential mechanisms (hypertension, obesity, obstructive sleep apnea, inflammation, endurance sports…).
Atrial remodeling and fibrosis development are associated with a variety of electric disturbances, such as heterogeneities in atrial action potential duration, effective refractory period, and conduction velocity2. These phenomena can promote and sustain AF.
Left atrial (LA) scarring can be detected by late enhancement MRI (MRI-DE) and can be correlated well with reduced electrogram amplitudes as recorded by endocardial voltage maps3. However, MRI to assess atrial fibrosis is not available in all centers due to its complex evaluation.
Electroanatomic mapping (EAM) can provide information regarding local voltage abnormalities that may be used as a surrogate marker for fibrosis. Specific voltage cut-off values have been reproducibly shown to accurately identify scar and/or fibrosis in the ventricles,4,5. EAM voltage cut-off values to identify myocardial scars in the atrial tissue are not as well defined as in the ventricle. Voltage-guided AF substrate modification targeting low voltage areas (LVA) has been carried out in some studies to improve long-term AF ablation efficacy 6-11. In most of them mapping has been performed using voltage cut-offs during sinus rhythm (SR), and in one study mapping was performed during AF11. However, a recent study has documented that the correlation between low-voltage and posterior LA MRI-DE is significantly improved when acquired during AF vs. sinus rhythm12.
The aim of our study was to evaluate the LVA extent and location in patients with persistent AF undergoing pulmonary veins isolation, and compare the findings on maps obtained in SR and AF in each patient.